Above-threshold ionization photoelectron spectrum from quantum trajectory

Many nonlinear quantum phenomena of intense laser-atom physics can be intuitively explained with the concept of trajectory. In this paper, Bohmian mechanics (BM) is introduced to study a multiphoton process of atoms interacting with the intense laser field: above-threshold ionization (ATI). Quantum trajectory of an atomic electron in intense laser field is obtained from the Bohm-Newton equation first and then the energy of the photoelectron is gained from its trajectory. With energies of an ensemble of photoelectrons, we obtain the ATI spectrum which is consistent with the previous theoretical and experimental results. Comparing BM with the classical trajectory Monte-Carlo method, we conclude that quantum potential may play a key role to reproduce the spectrum of ATI. Our work may present a new approach to understanding quantum phenomena in intense laser-atom physics with the image of trajectory.Comment: 10 pages, 3 figure

The Vlasov-Poisson-Landau System in Rx3\R^3_x

For the Landau-Poisson system with Coulomb interaction in $\R^3_x$, we prove the global existence, uniqueness, and large time convergence rates to the Maxwellian equilibrium for solutions which start out sufficiently close.Comment: 50 page

Electrochemical generation of catalytically active edge sites in c2n-type carbon materials for artificial nitrogen fixation

The electrochemical nitrogen reduction reaction (NRR) to ammonia (NH3) is a potentially carbon-neutral and decentralized supplement to the established Haber–Bosch process. Catalytic activation of the highly stable dinitrogen molecules remains a great challenge. Especially metal-free nitrogen-doped carbon catalysts do not often reach the desired selectivity and ammonia production rates due to their low concentration of NRR active sites and possible instability of heteroatoms under electrochemical potential, which can even contribute to false positive results. In this context, the electrochemical activation of nitrogen-doped carbon electrocatalysts is an attractive, but not yet established method to create NRR catalytic sites. Herein, a metal-free C2N material (HAT-700) is electrochemically etched prior to application in NRR to form active edge-sites originating from the removal of terminal nitrile groups. Resulting activated metal-free HAT-700-A shows remarkable catalytic activity in electrochemical nitrogen fixation with a maximum Faradaic efficiency of 11.4% and NH3 yield of 5.86 µg mg−1cat h−1. Experimental results and theoretical calculations are combined, and it is proposed that carbon radicals formed during activation together with adjacent pyridinic nitrogen atoms play a crucial role in nitrogen adsorption and activation. The results demonstrate the possibility to create catalytically active sites on purpose by etching labile functional groups prior to NRR

Endothelin receptor B antagonists decrease glioma cell viability independently of their cognate receptor

Background: Endothelin receptor antagonists inhibit the progression of many cancers, but research into their influence on glioma has been limited. Methods: We treated glioma cell lines, LN-229 and SW1088, and melanoma cell lines, A375 and WM35, with two endothelin receptor type B (ETRB)-specific antagonists, A-192621 and BQ788, and quantified viable cells by the capacity of their intracellular esterases to convert non-fluorescent calcein AM into green-fluorescent calcein. We assessed cell proliferation by labeling cells with carboxyfluorescein diacetate succinimidyl ester and quantifying the fluorescence by FACS analysis. We also examined the cell cycle status using BrdU/propidium iodide double staining and FACS analysis. We evaluated changes in gene expression by microarray analysis following treatment with A-192621 in glioma cells. We examined the role of ETRB by reducing its expression level using small interfering RNA (siRNA). Results: We report that two ETRB-specific antagonists, A-192621 and BQ788, reduce the number of viable cells in two glioma cell lines in a dose- and time-dependent manner. We describe similar results for two melanoma cell lines. The more potent of the two antagonists, A-192621, decreases the mean number of cell divisions at least in part by inducing a G2/M arrest and apoptosis. Microarray analysis of the effects of A-192621 treatment reveals up-regulation of several DNA damage-inducible genes. These results were confirmed by real-time RT-PCR. Importantly, reducing expression of ETRB with siRNAs does not abrogate the effects of either A-192621 or BQ788 in glioma or melanoma cells. Furthermore, BQ123, an endothelin receptor type A (ETRA)-specific antagonist, has no effect on cell viability in any of these cell lines, indicating that the ETRB-independent effects on cell viability exhibited by A-192621 and BQ788 are not a result of ETRA inhibition. Conclusion: While ETRB antagonists reduce the viability of glioma cells in vitro, it appears unlikely that this effect is mediated by ETRB inhibition or cross-reaction with ETRA. Instead, we present evidence that A-192621 affects glioma and melanoma viability by activating stress/DNA damage response pathways, which leads to cell cycle arrest and apoptosis. This is the first evidence linking ETRB antagonist treatment to enhanced expression of DNA damage-inducible genes

Obvious enhancement of the total reaction cross sections for 27,28^{27,28}P with 28^{28}Si target and the possible relavent mechanisms

The reaction cross sections of $^{27,28}$P and the corresponding isotones on Si target were measured at intermediate energies. The measured reaction cross sections of the N=12 and 13 isotones show an abrupt increase at $$. The experimental results for the isotones with $Z\leq 14$ as well as $$P can be well described by the modified Glauber theory of the optical limit approach. The enhancement of the reaction cross section for $^{28}$P could be explained in the modified Glauber theory with an enlarged core. Theoretical analysis with the modified Glauber theory of the optical limit and few-body approaches underpredicted the experimental data of $^{27}$P. Our theoretical analysis shows that an enlarged core together with proton halo are probably the mechanism responsible for the enhancement of the cross sections for the reaction of $^{27}$P+$^{28}$Si.Comment: 16 pages, 5 figures, to be published in Phys.Rev.

Altered resting-state functional activity in posttraumatic stress disorder: A quantitative meta-analysis

Many functional neuroimaging studies have reported differential patterns of spontaneous brain activity in posttraumatic stress disorder (PTSD), but the findings are inconsistent and have not so far been quantitatively reviewed. The present study set out to determine consistent, specific regional brain activity alterations in PTSD, using the Effect Size Signed Differential Mapping technique to conduct a quantitative meta-analysis of resting-state functional neuroimaging studies of PTSD that used either a non-trauma (NTC) or a trauma-exposed (TEC) comparison control group. Fifteen functional neuroimaging studies were included, comparing 286 PTSDs, 203 TECs and 155 NTCs. Compared with NTC, PTSD patients showed hyperactivity in the right anterior insula and bilateral cerebellum, and hypoactivity in the dorsal medial prefrontal cortex (mPFC); compared with TEC, PTSD showed hyperactivity in the ventral mPFC. The pooled meta-analysis showed hypoactivity in the posterior insula, superior temporal, and Heschl's gyrus in PTSD. Additionally, subgroup meta-analysis (non-medicated subjects vs. NTC) identified abnormal activation in the prefrontal-limbic system. In meta-regression analyses, mean illness duration was positively associated with activity in the right cerebellum (PTSD vs. NTC), and illness severity was negatively associated with activity in the right lingual gyrus (PTSD vs. TEC)

Depinning of domain walls in permalloy nanowires with asymmetric notches

E ective control of the domain wall (DW) motion along the magnetic nanowires is of great importance for fundamental research and potential application in spintronic devices. In this work, a series of permalloy nanowires with an asymmetric notch in the middle were fabricated with only varying the width (d) of the right arm from 200 nm to 1000 nm. The detailed pinning and depinning processes of DWs in these nanowires have been studied by using focused magneto-optic Kerr e ect (FMOKE) magnetometer, magnetic force microscopy (MFM) and micromagnetic simulation. The experimental results unambiguously exhibit the presence of a DW pinned at the notch in a typical sample with d equal to 500 nm. At a certain range of 200 nm < d < 500 nm, both the experimental and simulated results show that the DW can maintain or change its chirality randomly during passing through the notch, resulting in two DW depinning elds. Those two depinning elds have opposite d dependences, which may be originated from di erent potential well/barrier generated by the asymmetric notch with varying d

Energy level alignment at Alq3/La0.7Sr0.3MnO3 interface for organic spintronic devices

The electronic structure of the interface between Tris (8-hydroxyquinolino)-aluminum (Alq3) and La0.7Sr0.3MnO3 manganite (LSMO) was investigated by means of photoelectron spectroscopy. As demonstrated recently this interface is characterized by efficient spin injection in organic spintronic devices. We detected a strong interface dipole of about 0.9 eV that shifts down the whole energy diagram of the Alq3 with respect to the vacuum level. This modifies the height of the barriers for the holes injection to 1.7 eV, indicating that hole injection from LSMO into Alq3 is more difficult than it was expected as the energy level matched by vacuum levels. We believe the interface dipole is due to the intrinsic dipole moment characteristic for Alq3 layer. An additional weak interaction is observed between the two materials influencing the N 1s core levels of the organic semiconductor. The presented data are of greatest importance for both qualitative and quantitative description of the organic spin valves.Comment: 17 pages, 4 figure

Size and shape evolution of embedded single-crystal αα-Fe nanowires

The size and shape evolution of embedded ferromagnetic αα-Fe nanowires is discussed. The αα-Fe nanowires are formed by pulsed-laser deposition of La0.5Sr0.5FeO3−xLa0.5Sr0.5FeO3−x on single-crystal SrTiO3SrTiO3 (001) substrate in reducing atmosphere. The average diameter of the nanowires increases from d ≈ 4d≈4 to 50 nm as the growth temperature increases from T = 560T=560 to 840 °C. Their in-plane shape evolves from circular to octahedral and square shape with [110] facets dominating as the growth temperature increases. A fitting to a theoretical calculation shows that the circular shape is stable when the diameter of the nanowires is smaller than 8 nm.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/87835/2/203110_1.pd

Tim-3 Negatively Regulates IL-12 Expression by Monocytes in HCV Infection

T cell immunoglobulin and mucin domain-containing protein 3 (Tim-3) is a newly identified negative immunomodulator that is up-regulated on dysfunctional T cells during viral infections. The expression and function of Tim-3 on human innate immune responses during HCV infection, however, remains poorly characterized. In this study, we report that Tim-3 is constitutively expressed on human resting CD14+ monocyte/macrophages (M/MØ) and functions as a cap to block IL-12, a key pro-inflammatory cytokine linking innate and adaptive immune responses. Tim-3 expression is significantly reduced and IL-12 expression increased upon stimulation with Toll-like receptor 4 (TLR4) ligand - lipopolysaccharide (LPS) and TLR7/8 ligand - R848. Notably, Tim-3 is over-expressed on un-stimulated as well as TLR-stimulated M/MØ, which is inversely associated with the diminished IL-12 expression in chronically HCV-infected individuals when compared to healthy subjects. Up-regulation of Tim-3 and inhibition of IL-12 are also observed in M/MØ incubated with HCV-expressing hepatocytes, as well as in primary M/MØ or monocytic THP-1 cells incubated with HCV core protein, an effect that mimics the function of complement C1q and is reversible by blocking the HCV core/gC1qR interaction. Importantly, blockade of Tim-3 signaling significantly rescues HCV-mediated inhibition of IL-12, which is primarily expressed by Tim-3 negative M/MØ. Tim-3 blockade reduces HCV core-mediated expression of the negative immunoregulators PD-1 and SOCS-1 and increases STAT-1 phosphorylation. Conversely, blocking PD-1 or silencing SOCS-1 gene expression also decreases Tim-3 expression and enhances IL-12 secretion and STAT-1 phosphorylation. These findings suggest that Tim-3 plays a crucial role in negative regulation of innate immune responses, through crosstalk with PD-1 and SOCS-1 and limiting STAT-1 phosphorylation, and may be a novel target for immunotherapy to HCV infection